What is the lowest dose of aspirin for maximum suppression of in vivo thromboxane production after a transient ischemic attack or ischemic stroke?
Cerebrovascular Diseases , Volume 17 - Issue 4 p. 296- 302
Background: There is still worldwide disagreement about the optimal lowest dose of aspirin to be used in patients after a transient ischemic attack (TIA) or nondisabling stroke. We measured the urinary 11-dehydrothromboxane-B 2 (uTXB2 excretion to compare the degree of suppression of in vivo platelet activation by various low doses of aspirin. Methods: 60 patients were randomly allocated to treatment with either 30, 50, 75 or 325 mg of aspirin. All patients received a 413-mg loading dose of carbasalate calcium (equivalent to 325 mg of aspirin) on day 0. The study population was stratified into a subgroup with acute ischemic stroke (AIS; n = 20; onset of symptoms <48 h) and a subgroup with a recent TIA or minor stroke (TIA/mS; n = 40) with onset of symptoms beyond 30 days, but less than a year previously. Urine samples were collected on day 0, 1, 5, 11 and 28 in patients with AIS, and on day 0, 11 and 28 in the patients with a TIA/mS. Results: On day 28, mean uTXB2 levels were 241, 130, 217 and 187 pmol/mmol creatinine in the four treatment groups (ANOVA, p = 0.43). In the AIS subgroup, uTXB2 remained suppressed on days 5 and 11 in all except the patients with the lowest dose (mean uTXB2 on days 5 and 11: 475 and 392 pmol/mmol creatinine; log-transformed ANOVA, p = 0.05). Conclusion: In patients with a TIA or nondisabling stroke, a daily dose of 30 mg of aspirin provides sufficient suppression of thromboxane synthesis. No indication of a dose-effect relationship was found. However, whether such a low dose adequately suppresses thromboxane synthesis in patients with acute stroke is uncertain. Copyright
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|Organisation||Department of Neurology|
Dippel, D.W.J, van Kooten, F, Leebeek, F.W.G, van Vliet, H.H.D.M, Mehicevic, A, Li, S.S.C, & Koudstaal, P.J. (2004). What is the lowest dose of aspirin for maximum suppression of in vivo thromboxane production after a transient ischemic attack or ischemic stroke?. Cerebrovascular Diseases, 17(4), 296–302. doi:10.1159/000077340